期刊
EXPERIMENTAL DERMATOLOGY
卷 20, 期 10, 页码 836-838出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1600-0625.2011.01324.x
关键词
beta-catenin; hydrogen peroxide; oxidative stress; premature senescence; human skin fibroblasts
类别
资金
- National Natural Science Foundation of China [30800992]
- Specialised Research Fund for the Doctoral Program of Higher Education [20100162110035]
- Natural Science Foundation of Hunan Province [10JJ9018]
- Scientific Research Fund of Hunan Provincial Science and Technology Department [2010FJ3155]
- Science Foundation of China Dermatologist Association-PG [2010CDA-PG04]
- Key Scientific Research Foundation of Nanhua Hospital, University of South China [10nyz01]
Oxidative stress is one of the most important causes of the cellular senescence process. Previous studies showed that beta-catenin can regulate FoxO3a and this association was enhanced in cells exposed to oxidative stress. It has also been reported that beta-catenin can regulate some senescence-related proteins. We propose that beta-catenin may play a crucial role in senescence of normal human primary skin fibroblasts (NHSFs). Here, we explored the roles and mechanisms of beta-catenin on H(2)O(2)-induced senescence in NHSFs. beta-catenin expression was decreased in NHSFs after H(2)O(2) treatment. Overexpression of beta-catenin in NHSFs led to a marked delay of many senescent phenotypes induced by H(2)O(2). Furthermore, overexpression of beta-catenin in NHSFs can antagonise the alteration of reactive oxygen species accumulation and some senescence-related proteins expression induced by H(2)O(2) treatment. Our data demonstrated that beta-catenin can protect NHSFs from H(2)O(2)-induced premature senescence by alleviating oxidative stress and regulating some senescence-related molecules.
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